Published animal and human studies support our hypothesis that fructose is a risk factor for NAFLD and NAFLD-related liver disease progression. In animal models, diets high in fructose induce features of the metabolic syndrome including weight gain, insulin resistance, hypertriglyceridemia, and hypertension. Similar effects are not observed with the administration of other simple sugars such as glucose. Fructose (or sucrose) administration to humans also causes features of metabolic syndrome which are quite typical of patients with NAFLD. Fructose is lipogenic, stimulates triglyceride synthesis and causes hepatic steatosis. As previously reported in animals, our group reported that increased fructose consumption (assessed as fructose-containing beverages only) is a risk factor of metabolic syndrome and biopsy-proven NAFLD and that patients with NAFLD consume 3-4 times more fructose than age, gender, and mass index (BMI) matched controls without liver disease.